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천이금속 표면에서의 수소 흡입의 동력학 : 수소흡착, 방출과 확산에 관하여
손기수,박동수,최상돈,김석환,배준규 慶北大學校 物理化學硏究所 1986 硏究論文集 Vol.7 No.-
천이금속(Nb) 표면에 수소의 두 상태는 R.J. Smith에 의해 암시되어 왔다. 우리는 이것을 받아들여 천이금속 표면에 두 개의 상태를 가정하여 몇 개의 경우의 potential barrier에 관해 charging과 degassing 조건하에서 수소원자의 fraction의 시간에 대한 변화율을 얻었다. 그리고 수소의 표면 fraction θ에 대해 온도와 log(θ/1-θ)의 비와 peak amplitude를 구하여 R.J. Smith팀의 실험결과와 비교했으며 그것을 이용해서 온도에 관한 desorption rate를 얻었다. It was known by R.J. Smith that there are two kinds of surface states on transition metal(Nb) surfaces. Furthermore for all metals desorption energy is larger than the solution energy. Here we present a model for hydrogen absorption of metal surfaces and then obtained the time rates of hydrogen charging and degassing on metal surfaces for few limiting cases. We also get log(θ/1-θ) versus the reciprocal temperature and peak amplitude of surface fraction versus the temperature, turned out to be good agreement with experiments. Finally we get the desorption fraction of hydrogen atom.
최석준 ( Suck Jun Choi ),채정룡 ( Jeong Ryong Chae ),문용식 ( Yong Shig Moon ),최태석 ( Tae Suck Choi ),심미령 ( Mi Ryeong Sim ),최석채 ( Suck Chei Choi ) 한국운동영양학회 2004 Physical Activity and Nutrition (Phys Act Nutr) Vol.8 No.2
The purpose of this study was to determine the effect of long distance running on the level of gastrointestinal hormones such as gastrin which stimulates the secretion of gastric acid, insulin and glucagon which affect glucose metabolism as well as the level of glucose. Method: Twenty four long distance runners (male 16, female 8) participated in this study. Studies were performed after an overnight fasting. The levels of gastrin, insulin, glucagon, and glucose in blood were measured at 30min before and after exercise, and then they were measured again at 24 hr after 10 km race. Result: Plasma gastrin level was increased immediately after exercise (p<0.05), while no significant changes were observed before and after 24 hours of exercise. Plasma insulin level was decreased immediately after exercise (p<0.05). Plasma glucagon level was elevated immediately after exercise (p<0.05). However, there was no significant difference in the level of plasma glucose level during the study period. Conclusion: These results indicate that the elevated level of gastrin in long distance runner may be involved in acid-related gastrointestinal disease. The changes of insulin and glucagon levels may represent the constant blood glucose level and further imply the fine regulatory mechanism of glucose homeostasis in blood during short time exercise in long distance runners.
Choi, Eun-Young,Park, Zee-Yong,Choi, Eun-Ju,Oh, Hyun-Mee,Lee, SungGa,Choi, Suck-Chei,Lee, Kang-Min,Im, Sin-Hyeog,Chun, Jang-Soo,Jun, Chang-Duk Wiley Subscription Services, Inc., A Wiley Company 2007 Journal of cellular biochemistry Vol.102 No.6
<P>We have shown that the bacterial iron chelator, deferoxamine (DFO), triggers inflammatory signals including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs) by activating the ERK1/2 and p38 kinase pathways. In this study we investigated the mechanisms involved in IL-8 generation by DFO, focusing on the transcription factors involved and the roles of both mitogen-activated protein kinases (MAPKs) in the transcription factor activation. Treatment of human epithelial HT-29 cells with DFO markedly up-regulated the expression of the essential components of the transcription factor AP-1 at a transcriptional level, while it minimally affected the expression of the NF-κB subunits. DFO also induced AP-1-dependent transcriptional activity in HT-29 cells, and this activity was further augmented by the wild-type c-Jun transfection. In contrast, the AP-1 activity by DFO was markedly decreased by the dominant-negative c-Jun transfection. Electrophoretic mobility shift assays revealed that DFO increases the specific binding of AP-1 but not of NF-κB. Such AP-1 binding and transcriptional activities were blocked by the inhibitors of the ERK1/2 and p38 kinase pathways, suggesting that both mitogen-activated protein kinases (MAPKs) lie upstream of AP-1. Besides its action on AP-1, DFO also induced the specific binding of other transcription factors such as CREB and Egr-1. In summary, our results indicate that iron chelator-induced IL-8 generation in IECs involves activation of ERK1/2 and p38 kinase and downstream activation of AP-1. A possible link between iron status and two additional transcription factors, that is, CREB and Egr-1, rather than NF-κB, was also suggested. J. Cell. Biochem. 102: 1442–1457, 2007. © 2007 Wiley-Liss, Inc.</P>
Choi, Suck-Chei,Han, Weon-Cheol,Park, Do-Sim,Kim, Eun-Cheol,Oh, Hyun-Mee,Oh, Jung-Mi,Jun, Chang-Duk The Korean Society for Microbiology 2002 Journal of Bacteriology and Virology Vol.32 No.1
Intercellular adhesion molecule-1 (ICAM-1) is a membrane protein, exists as a dimer on the cell surface, and interacts with leukocyte function associated antigen-1 (LFA-1), a member of ${\beta}_2$-integrin family. A soluble circulating form of ICAM-1 (sICAM-1) is also detected in human serum, and has been implicated as a regulator for LFA-1-dependent cell-cell interaction in vivo. However, previous reports demonstrated that sICAM-1 shows little inhibitory effect on LFA-1 binding to ICAM-1, indicating that sICAM-1 is unlikely to antagonize LFA-1/ICAM-1-mediated cellular events in vivo. Here, we investigated the property of the dimeric sICAM-1 as an inhibitor of LFA-1 interaction with ICAM-3, since the lower avidity of LFA-1 for ICAM-3 compared with ICAM-1 or ICAM-2 had been speculated. Using recently constructed heterodimeric sICAM-1 joined at the C terminus via an ${\alpha}$-helical coiled coil (ACID-BASE) (Jun, CD. et al., 2001, Proc Natl Acad Sci 98, 6830-6835), we also tested whether the structural integrity in dimer could affect the inhibitory action of sICAM-1. Engineered sICAM-1 dimer that contained intact ectodomain (E34/E34) significantly blocked SKW3 cell (LFA-$1^+$) binding to ICAM-3, but not to ICAM-1 and ICAM-2, indicating the lower avidity of LFA-1 to ICAM-3 than that of both ICAM-1 and ICAM-2. A one binding site knock out mutant (E34/K34) showed ${\sim}2$-fold reduction in efficiency compared with E34/E34 to inhibit cell binding. Interestingly, a one binding domain deletion mutant (E34/${\Delta}D1$-D2) showed significant reduction (${\sim}5$-fold) compare with E34/K34, suggesting that structural integrity, which is precluded in E34/${\Delta}D1$-D2, is necessary for optimal binding of dimeric sICAM-1 to LFA-1, thereby inhibiting LFA-1/ICAM-3-dependent adhesion. Furthermore, BIAcore affinity measurements revealed that E34/${\Delta}D1$-D2 bound to immobilized soluble open LFA-1 I domain with an ${\sim}3$-fold reduced affinity compared with E34/K34. Overall, our results demonstrate that maintaining the structural integrity in dimer is necessary for optimal binding of sICAM-1 to LFA-1, and further suggest the therapeutic potential of dimeric sICAM-1 to antagonize LFA-1/ICAM-3-mediated cellular events in vivo.
Choi, Suck-Chei,Choi, Eun-Ju,Oh, Hyun-Mee,Lee, SungGa,Lee, Jeong-Kun,Lee, Meung-Su,Shin, Yong-Il,Choi, Suck-Jun,Chae, Jeong-Ryong,Lee, Kang-Min,Lee, Won-Jung,Park, Jae-Sik,Shin, Chang-Yell,Oh, Tae-You WJG Press 2006 WORLD JOURNAL OF GASTROENTEROLOGY Vol.12 No.30
<P>To investigate whether, or how, DA-9601, which is a new gastroprotective agent, inhibits TNF-alpha-induced inflammatory signals in gastric epithelial AGS cells.</P>
Jun, Chang-Duk,Kim, Yurim,Choi, Eun-Yong,Kim, Minsun,Park, Byungrim,Youn, Byungsoo,Yu, Kangyeol,Choi, Kyu-Sil,Yoon, Kwon-Ha,Choi, Suck-Chei,Lee, Myeung-Su,Park, Kie-In,Choi, Minkyu,Chung, Yeuntai,Oh, Crohn's Colitis Foundation of America, Inc. 2006 Inflammatory bowel diseases Vol.12 No.7
BACKGROUND:: Gliotoxin, a fungal metabolite, has been known to show strong immunosuppressive properties, although its mechanisms are not completely understood. In this report, the authors investigated the mechanism whereby gliotoxin has anti-inflammatory properties in vitro and in trinitrobenzene sulfonic acid-induced colitis. MATERIALS AND METHODS:: Body weight, histological scores, and myeloperoxidase activity were evaluated in trinitrobenzene sulfonic acid colitis. Nuclear factor-&kgr;B (NF-&kgr;B) p65, tumor necrosis factor-α, interleukin (IL)-1&bgr;, IL-12, and intercellular adhesion molecule-1 were detected by immunohistochemical staining. IL-8 secretion was measured by an enzyme-linked immunosorbent assay. Heme oxygenase-1 (HO-1) expression and I-&kgr;B degradation were analyzed by Western blot. RESULTS:: Pretreatment of human epithelial HT-29 cells with gliotoxin significantly blocked the I-&kgr;B degradation and NF-&kgr;B p65 nuclear translocation induced by tumor necrosis factor-α or IL-1&bgr;; these were parallel with the inhibition of IL-8 secretion and intercellular adhesion molecule-1 expression in the same cells. Interestingly, gliotoxin induced HO-1 in HT-29 cells and, in turn, inhibition of HO-1 activity by a zinc protoporphyrin IX reversed the effects of gliotoxin in terms of I-&kgr;B degradation, intercellular adhesion molecule-1 expression, and IL-8 production. In trinitrobenzene sulfonic acid colitis, gliotoxin administration significantly improved the clinical and histopathological symptoms. Notably, gliotoxin also induced HO-1 in the colonic mucosa and zinc protoporphyrin IX reversed the protective effects of gliotoxin in trinitrobenzene sulfonic acid colitis. CONCLUSIONS:: These results demonstrate for the first time that the anti-inflammatory actions mediated by gliotoxin include HO-1 induction and the subsequent blockade of NF-&kgr;B-dependent signaling pathways in vitro and in vivo. The current results also demonstrate that gliotoxin may be an effective agent for the treatment of diseases characterized by mucosal inflammation.